Evidence map›Paper›PMID 33666815›Full record

ArticleCell stress & chaperones2021

Urolithin A induces cell cycle arrest and apoptosis by inhibiting Bcl-2, increasing p53-p21 proteins and reactive oxygen species production in colorectal cancer cells.

Mohammad S El-Wetidy, Rehan Ahmad, Islam Rady, Hamed Helal, Mohamad I Rady, Mansoor-Ali Vaali-Mohammed, Khayal Al-Khayal, Thamer Bin Traiki, Maha-Hamadien Abdulla

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell stress & chaperones, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 3 countries.

Mohammad S El-Wetidy *Zoology Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo, 11823, Egypt.
Rehan Ahmad *Colorectal Research Chair, Department of Surgery, College of Medicine, King Saud University, PO Box 7805 (37), Riyadh, 11472, Kingdom of Saudi Arabia. arehan@ksu.edu.sa.
Islam RadyZoology Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo, 11823, Egypt.
Hamed HelalZoology Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo, 11823, Egypt.
Mohamad I RadyZoology Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo, 11823, Egypt.
Mansoor-Ali Vaali-MohammedColorectal Research Chair, Department of Surgery, College of Medicine, King Saud University, PO Box 7805 (37), Riyadh, 11472, Kingdom of Saudi Arabia.
Khayal Al-KhayalColorectal Research Chair, Department of Surgery, College of Medicine, King Saud University, PO Box 7805 (37), Riyadh, 11472, Kingdom of Saudi Arabia.
Thamer Bin TraikiColorectal Research Chair, Department of Surgery, College of Medicine, King Saud University, PO Box 7805 (37), Riyadh, 11472, Kingdom of Saudi Arabia.
Maha-Hamadien AbdullaColorectal Research Chair, Department of Surgery, College of Medicine, King Saud University, PO Box 7805 (37), Riyadh, 11472, Kingdom of Saudi Arabia. mabdulla@ksu.edu.sa.
King Saud University · SAAl-Azhar University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the second most common gastrointestinal cancer globally. Prevention of tumor cell proliferation and metastasis is vital for prolonging patient survival. Polyphenols provide a wide range of health benefits and prevention from cancer. In the gut, urolithins are the major metabolites of polyphenols. The objective of our study was to elucidate the molecular mechanism of the anticancer effect of urolithin A (UA) on colorectal cancer cells. UA was found to inhibit the cell proliferation of CRC cell lines in a dose-dependent and time-dependent manner in HT29, SW480, and SW620 cells. Exposure to UA resulted in cell cycle arrest in a dose-dependent manner along with alteration in the expression of cell cycle-related protein. Treatment of CRC cell lines with UA resulted in the induction of apoptosis. Treatment of HT29, SW480, and SW620 with UA resulted in increased expression of the pro-apoptotic proteins, p53 and p21. Similarly, UA treatment inhibited the anti-apoptotic protein expression of Bcl-2. Moreover, exposure of UA induced cytochrome c release and caspase activation. Furthermore, UA was found to generate reactive oxygen species (ROS) production in CRC cells. These findings indicate that UA possesses anticancer potential and may be used therapeutically for the treatment of CRC.

Indexed as

Antineoplastic AgentsApoptosisCaspase 3Cell Cycle CheckpointsCell DeathCell Line, TumorCell ProliferationColorectal NeoplasmsHumansProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesTumor Suppressor Protein p53Antineoplastic AgentsBCL2 protein, humanCaspase 3Proto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesTumor Suppressor Protein p53ApoptosisCell cycle arrestColorectal cancerReactive oxygen speciesUrolithin A

Identifiers

PMID33666815
PMCPMC8065090
OpenAlexW3134124522

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.